Experiments will be performed in the intact anesthetized dog and also in isolated cardiac tissues to determine the basic electrophysiology of automaticity. Using both extracellular and intracellular techniques electrical activity will be recorded from multiple sites within the heart. Premature beats and overdrive suppression will be used to determine the responses of normal pacemakers located in the sinus node, ectopic atrial sites, the bundle of His or ectopic ventricular sites with and without enhanced automatic tone. Abnormal automaticity will be induced by digitalis intoxication and acute coronary artery ligation. Using the same techniques the characteristics of this abnormal automaticity will be evaluated in the several pacemaker tissues and contrasted with the normal automaticity. Using microelectrode techniques to record transmembrane potentials from the isolated tissues the basic electrophysiology underlying the pacemaer responses will be elucidated. The data generated by these experiments will provide information relevant to mechanisms of various cardiac arrhythmias including sinus node bradycardia, sinus arrest, bradycardia-tachycardia syndrome, sinus node exit block, sinus node reentry, junctional tachycardia, ventricular tachycardia, wandering pacemaker, coupled rhythms, and bradycardia-dependent conduction block. BIBLIOGRAPHIC REFERENCES: Spear, J. F. Patterns of ventricular activation during ventricular arrhythmias 24 hours following experimental myocardial infarction. In: Pathophysiology and Therapeutics of Ischemia. (In Press), 1977. Moore, E. N. and Spear, J. F. Origin of ventricular arrhythmias in 24 hour old septal and anterior infarcts studied by epicardial and intramural mapping. In: Reentrant Arrhythmias (In Press), 1977.